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FEBS Lett. 1999 Jul 23;455(3):315-20.

Induction of apoptosis by human amylin in RINm5F islet beta-cells is associated with enhanced expression of p53 and p21WAF1/CIP1.

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1
The School of Biological Sciences, University of Auckland, New Zealand.

Abstract

Human amylin (10 microM) significantly inhibited RINm5F islet beta-cell proliferation and evoked apoptosis associated with typical degenerative ultrastructural changes and DNA fragmentation, whereas rat amylin did not. Time course analysis showed that human amylin elicited apoptosis in a passage-dependent manner. Expression of the apoptosis-related genes p53, bcl-2 and WAF1/CIP1 was examined using Northern blots. mRNAs corresponding to p53 and to p21WAF/CIP1 were remarkably increased following human amylin treatment, whereas no change in bcl-2 was detected. Our data suggest a role of p53 and p21 in human amylin-induced beta-cell apoptosis. Furthermore, cells with higher proliferative potential (lower passage) were found to be more susceptible to apoptosis and to induction of p53, suggesting that beta-cells with different proliferation rates respond differently to human amylin, and that human amylin may be more toxic to proliferating cells.

PMID:
10437796
DOI:
10.1016/s0014-5793(99)00894-7
[Indexed for MEDLINE]
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